the influence of atrial systole on ventricular capture by failing artificial pacemakers. ii....

The influence of atrial systole on ventricular

capture by failing artificial pacemakers. II.

Experimental observations

William S. Abernathy, M.D. Gregory R. Ferrier, Ph.D. Gordon K. Moe, M.D., Ph.D. Utica, N. Y.

The efficacy of ventricular capture by failing artificial pacemakers can be influenced by atria1 activity. Twenty-six cases have been reviewed recently.’ Two hypotheses have been advanced to explain this phenomenon. One theory invokes an electrotonic interaction (Wedensky facilitation or inhibition) between the pacemaker stimulus and the atria1 depolarization. (The Wedensky effect is a separate phenomenon and is not considered in this report.) The other theory postulates that atria1 systole influences the efficacy of capture by altering the physical contact between the pacing electrode and the ventricular myocardium. The present study was undertaken to reproduce this phenomenon in the dog and to ascertain which of these two mechanisms was operative. The results strongly support the mechanical hypothesis.

Methods

Mongrel dogs of either sex, weighing 10 to 23 kilograms, were anesthetized with sodium pento- barbital (30 mg./Kg., intravenously) and given additional doses as required. Following a right thoracotomy, the heart was suspended in a peri- cardial cradle. In some dogs the right upper lobe of the lung was excised to facilitate exposure. A Harvard respirator provided ventilation.

Atrioventricular block was created in one of

From the Masonic Medical Research Laboratory, Utica, N. Y. Supported in part by grant HL-19487, National Heart, Lung and Blood Institute.

Received for publication Sept. 23, 1977.

Accepted for publication Nov. 17, 1977. Reprint requests William S. Abernathy, M.D., Masonic Medical Research Laboratory, Utica, N. Y. 13503.

two ways. The ends of two pieces of fine (0.006 inch diameter) Teflon-coated steel wire were bent to form hooks and were inserted through the right atria1 wall into the region of the His bundle. After recording a His bundle electrogram to verify the position, a strong electric shock (20 to 150 joules) was passed through the heart using both wires as one pole and a large (8.7 cm. diameter) metal paddle applied to the left ventricle as the other pole.* Complete heart block was achieved in six dogs, and first degree block (A-V = 139 to 149 msec.) in one dog. Complete heart block was produced in an additional five dogs by injecting formalin into the His bundle.”

The mid-right atrium was paced through a close bipolar epicardial electrode. The right ventricle was stimulated through a transvenous bipolar pacing catheter (USC1 No. 007152); the position of this catheter in the right ventricle was adjusted by trial and error until atria1 systole exerted an influence on the test stimulus. All stimuli were of 3 msec. duration and were passed through isolation transformers. The strength of all stimuli except the ventricular test stimulus (Vs’) was two to three times threshold.

Fig. 1 illustrates the stimulation patterns employed in this study. The atrium and ventricle were sequentially paced with a delay of 100 msec. and with a train of 9 to 20 (usually 10) basic stimuli. In Fig. 1 the last of these are designated As,, VsB, As,,,, VqO. (Stimuli are denoted by the subscript “S”, and the corresponding beats are designated without the subscript; for example, stimulus As, gives rise to beat A,.) In any given experiment the cycle length of the basic stimuli

0502-8703/78/0495-048!3$00.80/0 0 1978 The C. V. Mosby Co. American Heart Journal 489

Abernathy, Ferrier, and Moe

Fig. 1. Stimulation patterns. Vertical lines above and below the horizontal line represent stimuli delivered to the atrium and ventricle, respectively. The strength of the teat stimulus (Vs’) was less than that of the basic stimuli (Va,, Vs,,). The broken l&es inpaneb A and B indicate that As’ and As” may assume various temporal positions. Tie calibration = 100 msec.

was constant; the cycle lengths of all the experiments varied-between 220 and 380 msec. (mean = 323 msec.). A ventricular test stimulus (Vs’) was then delivered at approximately the same interval as the basic stimuli; the teat stimulus was never premature enough to encroach upon a possible zone of supernormal excitability. The purpose of this test stimulus (Vs’) was to imitate a failing pacemaker; hence, the strength of Vs’ was adjusted to a value that was barely successful or barely unsuccessful in exciting the heart.

The influence of atria1 systole on the efficacy of Vs’ was studied by introducing one or more atria1 stimuli (As’, As”, As”‘) as illustrated in Fig. 1. The influence of atria1 systole on Vs’ was demonstrated as follows: In the control situation, no atria1 stimulus was delivered before Vs’, and an atria1 escape beat (AE) occurred after Vs’ (Fig. 1A). In the test situation, a single atria1 stimulus (As’) was delivered at a variable interval before Vs’ (Fig. 1A). The phenomenon under study was present when a suitably timed atria1 beat (A’) changed the excitatory efficacy of Vs’ as compared to control (no As’).

The mechanism of this phenomenon was investigated by altering the hemodynamic performance of the atrial beat (A’) immediately preceding Vs’. The purpose of these experiments was to dissociate partially the hemodynamic and electrotonic effects of A’. Fig. 1B shows a sequence that decreased the strength of the contraction of A’ as reflected by the right atria1 pressure. Holding As’ in a fixed temporal position, another atria1 stimulus (As”) was interpolated at various times after the last basic beat (Fig. 1B). In other

A’ v. t

&[

10

0 0

-250

Fii. 2. Facilitation of Vs’ and interpolation of A”. In each panel, top line = atria1 electrogram; midd& line = electrocardiogram; bottom line = right atria1 pressure. Panel A: control. Panel 33: facilitation (A’-%’ = 88 msec). Panel C: interpolation of A” (A’-Vs’ i= 99 msec A”-A’ = 152 maec.). The figures were traced from original photographs. The records of the ventricular stimuli were omitted. Time calibration @&row) = 250 maec. Pressure calibrations (right) = 0 to 10 mm Hg. Experiment performed on March 2, 1977.

experiments, the contraction of A’ was enhanced by interpolating an atria1 stimulus (As”‘) in the penultimate diastole (Fig. 1C). The position of As”’ was held constant, and the position of As’ was usually, but not always, fixed.

That the excitatory efficacy of Vs’ was in fact being influenced by A’ was verified repeatedly. After at most every tenth Vs’, the atria1 stimulation sequence was changed in such a way that the efhcacy of Vs’ should change too. For example, if Vs’ excited the ventricle with A’ preceding Vs’ by 100 msec., then non-capture by Vs’ in the absence of A’ was confkned regularly. Data were accepted for analysis only if such a reversal of effect occurred within four test cycles.

Early in the study it became apparent that respiration had an independent effect on the efficacy of Vs’. This effect was characterized by failure of capture on inspiration and was probably caused by movement of the heart or catheter. To compensate for this respiratory effect, all Vs{ were

490 April, 1978, Vol. 95, No. 4

Atriul systole and failing pacemakers

delivered at the end of expiration. This was accomplished by matching the number and cycle length of the basic stimuli to the respiratory rate. The timing was checked by means of an electrical signal elicited from the respirator at the onset of inspiration.

In all experiments a standard lead electrocardiogram, a close bipolar mid-right atria1 electrogram, the ventricular stimuli, and the respiratory signal were recorded. The A’-Vs’ interval was measured from the intrinsic deflection of the atria1 electrogram to the test stimulus. The A”-A’ interval was measured from one intrinsic deflection to the other. The capture by Vs’ was judged by examining the electrocardiogram for the presence or absence of a QRS immediately following Vs’.

Right atria1 pressure was measured through a transvenous catheter or through a large-bore (4.5 mm. internal diameter) copper tube inserted in the right atria1 appendage. These were connected to a Statham transducer (model P23BC) inter- faced with an Electronics for Medicine amplifier (model SGA). The transducer was calibrated against a mercury manometer. All pressures were measured at the time Vs’ occurred and were measured to the nearest 0.5 or 1.0 mm. Hg.

All data were recorded on a TEAC tape recorder (model R-351 F) and were later photo- graphed on continuously moving (25 mm./sec.) film with a Grass Kymograph camera (model C4- K). The photographic image was enlarged, and the data were measured with an accuracy of at least -+ 5 msec. Time calibrations were provided both by a digital interval generator (built by W. J. Mueller) and by a Tektronix interval generator (model 16OA).

The statistical tests used were Chi-squared derived from a contingency table with Yates’ correction where appropriate, Student’s t test for the difference of the means, and the Wilcoxon two sample test for the unpaired case.4

Raaults

Facilitation and inhibition of Vs’. Facilitation of ventricular capture by Vs’ is illustrated in Fig. 2. In the control state (Fig. 2A), Vs’ did not excite the ventricle when As’ was omitted, and an atria1 escape beat (AE) occurred after Vs’. In the test condition (Fig. 2B), Vs’ captured the ventricle when a single atria1 beat (A’) preceded Vs’ by 66 msec. Note that the right atria1 pressure coincident with Vs’ was low in the absence of A’ (Fig.

r-l N

Fig. 3. Facilitation of Vs’. Abscissa: the A’-Vs’ interval in msec. Data are plotted in 10 msec. groups; i.e., 0 to 10,ll to 20, 21 to 30, etc. “N” refers to data collected when As’ was omitted, and rin atria1 escape beat (AE) occurred after Vs’. Ordinate: the per cent of Vs’ that was successful in ventricular capture at any given A’-% interval. Total number of Vs’ = 666. Experiment performed on Apr. 14, 19,777.

2A) and high in the presence of A’ (Fig. 2.B). The time course of facilitation was examined by placing A’ at various times before Vs’. The results of one such experiment are shown in Fig. 3. When the A’-Vs’ interval was less than 41 msec. or greater than 110 msec., Vs’ did not excite the heart. However, when the A’-Vs’ interval was 41 to 110 msec., A’ facilitated ventricular capture by Vs’. Inhibition of ventricular capture was demonstrated in other experiments of the same design. In six dogs either facilitation or inhibition of ventricular capture could be alternatively elicited by changing the position of the pacing catheter in the ventricle; an example of this is presented in Fig. 4 in which all of the data are from the same dog. In this figure, A’ facilitated Vs’ when the A’- Vs’ interval was 51 to 140 msec., and A’ inhibited Vs’ when the interval was 61 to 170 msec. In most experiments, A’ affected the efficacy of Vs’ when the A’-Vs’ interval was 41-150 msec.; the narrowest effective range observed was 31 to 110 msec., and the widest effective range was 11 to 160 msec. Faster basic driving rates tended to give narrower ranges of effective A’-Vs’ intervals, but this observation was not systematically examined.

Experiments in which the efficacy of Vs’- was influenced by a single atria1 beat (A’) were performed in 11 dogs; facilitation was shown in seven, and inhibition in eight. Eleven complete curves similar to those shown in Figs. 3 and 4 were constructed from these experiments.

American Heart Journal 491


Fig. 4. Alternate facilitation and inhibition of Vs’ in the same dog. Abscissa and ordinate are identical to those in Fig. 3. (A): Facilitation, total number of Vs’ = 393. (0): Inhibition, total number of Vs’ = 863. Experiment performed on Mar. 29, 1977.

Interpolation experiments with weakening of the contraction of A’. In Fig. 2B, A’ facilitated Vs’. When an atria1 beat (A”) was interpolated immediately before A’, the facilitation was abol- ished, and Vs’ did not excite the ventricle (Fig. 2C). Another experiment of this type, but with opposite conditions, is shown in Fig. 5. In the control state (not illustrated), As’ and As” were omitted, and Vs’ excited the ventricle. In Fig. 5A, A’ alone inhibited ventricular capture by Vs’. However, when both A’ and A” were present (Fig. 5B), the inhibition disappeared, and Vs’ again excited the ventricle. In both experiments, interpolation of A” did not change the appearance of A’ on the electrocardiogram or electrogram, but this interpolation did impair greatly the hemodynamic performance of A’ as revealed by the lower pressure at the time Vs’ occurred (compare Figs. 2B and 2C, and Figs 5A and 5B). Fig. 5C confirms that A’ was hemodynamically ineffective in Fig. 5B.

Gradations in the extent of hemodynamic impairment of A’ were produced by varying the A”-A’ interval while holding the position of A’ constant. Fig. 6 illustrates the results of two such experiments. In Fig. 6A, in the control state (NO A’/A”), the strial pressure was low, and Vs’ did not excite the ventricle. In the first test condition (A’ ONLY), the pressure was high, and Vs’ captured the ventricle. When A” was interpolated at progressively shorter A/‘-A intervals (A”-A’ INTERVAL), the atria1 pressure generated by A’ fell toward the control value, and the facilitation of Vs’ by A’ was progressively eliminated. Following a change in the position of the pacing

Fig. 5. Inhibition of Vs’ and interpolation of A”. Data records and calibrations are the same aa in Fig. 2. Panel A: inhibition (A’-Vs’ = 95 msec.). Panel B: interpolation of A” (A’-Vs’ = 95 nwec., A”-A’ = 132 msec.). Panel C: A” alone (A”-,’ = 227 msec.). Traced from the original photographs. Experiment performed on March 2,1977.

catheter, the data in Fig. 6B were obtained from the same dog that was represented in Fig. 6A. Interpolating A” at decreasing A”-A’ intervals resulted in a progressive loss of the inhibition of Vs’ by A’ and a progressive fall in the atria1 pressure toward the control value (Fig. 6B). In both Figs. 6A and 6B, at short A”-A’ intervals the hemodynamic effect of A’ became negligible, and the efficacy of Vs’ approached that seen in the absence of both A” and A’. Moreover, the magni- tude of the influence of A’ varied directly with the pressure generated by A’.

Experiments of this type were done in five dogs; facilitation was reversed in four, and inhibition in four. Seven complete curves of the kind shown in Fig. 6 were constructed from the data.

At very short A”-As’ intervals ( < 150 msec.), either As’ failed to excite the atrium; or the As’-A’ latency increased, and A’ became grossly aberrant. Data were rejected from analysis if A’ was

492 April, 1978, Vol. 95, No. 4

Atrial systole and failing pacemakers

IA’1 I 190 I I I 1 1 11 1

ONLY 170 Eo

A’+! INTERVAL (“‘d A% TIbo’ ONLY k-b! INTERVAL W &A0

Fig. 6. Facilitation (panelA) and inhibition (panel B) of Vs’ and interpolation of A” (bothpanels). Abscissa: NO A’/A”: control. A’ ONLY: first test condition. A”-A’ INTERVAL: second teat condition, the time interval in msec.

between these beats.. Left ordinate (0): the per cent of Vs’ that was successful in ventricular capture at any given stimulation pattern. Right ordinate (0 ): the arithmetic average of all the right atria1 pressures recorded during any given stimulation pattern. In these experiments, the A’-Vs’ interval was constant at 100 msec. until the A”-A interval fell below 160 msec., at which point the A’-Vs’ interval was, 35 to 100 msec. Total number of Vs’ = 687 bane1 A) and 431 fpanel B). Experiment performed on March 28, 1977.

aberrant or if the A’-Vs.’ interval shortened by more than 15 msec. as compared to the initial test condition (A’ ONLY). In all dogs studied with an interpolated A”, a reduction of the pressure generated by A’ and a nullification of the effect of A’ on Vs’ were seen ,at A”-A’ intervals which produced no aberration of A’ and no change in the. A’-Vs’ interval.

Interpolation experiments with enhancement of the contraotion of A’. In some experiments the control condition was that the efficacy of Vs’ was not influenced by the presence, the timing (A’-Vs’ interval), or the absence of A’ alone (Fig. 7A).

However, when an atria1 beat (A”‘) was interpolated in the penultimate cycle, the hemodynamic force of A’ was enhanced, and A’ then exerted an effect on the efficacy of Vs’ (Fig. 7B). In Fig. 7A, the atria1 pressure at the time of Vs’ was the same as during the basic beats, and Vs’ did not excite the ventricle. In Fig. 7B, interpolation of A”’ caused an increase in the pressure generated by A’, and A’ then facilitated Vs’. The change in the efficacy of Vs’ was not due solely to the presence of A”‘. This was demonstrated in three dogs by changing the A’-Vs’ interval while leaving A”’ in a fixed position (not illustrated); Vs’ was influenced

American Heart Journ&l

only during a specific range of A’-Vs’ intervals (40 to 150 msec.).

The results of all the experiments of this type are summarized in Table I. (Experiments with a variable A’-Vs’ interval are excluded.) In all dogs, interpolation of A”’ significantly increased the pressure, generated by A’, and the hemodynami- tally enhanced A’ then significantly changed the efficacy of Vs’.

Atrial prbsure and efficacy of Vs’. There was an excellent correlation between the level of the atria1 pressure (coincident with Vs’) and the efficacy of Vs’ (Fig. 8). An increasing pressure was associated with greater facilitation or greater inhibition of Vs’ by A’. Moreover, the correlation between pressure and success (Fig. 8) was independent of the stimulation pattern employed. An increase in pressure was accomplished by an atria1 systole (A’) alone with suitable timing (A’- Vs’ intervals of approximately 40 to 150 msec.), by hemodynamically enhancing A’ with an interpolated beat (A”‘), or by an A’ with a long W-A’ interval. A decrease in pressure was achieved by omitting As’ so that an escape beat occurred after Vs’, by relatively short or long A’-Vs’ intervals, or by interpolating a beat (A”) at a suitable interval

493


Fig. 7. Facilitation of Vs’ when the contraction of A’ was enhanced by interpolation of A”‘. Data records are the same as in iQ. 2. Panel A: control. Panel B: interpoIation of A”‘. A’-%’ = 75 msec. in both panels. The right atria1 pressures coincident with Vs’ are indicated by the rmmbers at the ends of the broken lines. Traced from the original photographs. Time calibration (below) = 100 msec. Pressure calibrations (right) = 0.0 to 10.0 mm. Hg. Experiment performed on April 15, 1977.

immediately before A’. For example, the data in Fig. 8 came from experiments in one dog in which A’ alone was present at varying A’-Vs’ intervals, in which A’ was present with varying A/‘-A’ intervals, and in which As’ was omitted. In total, 10 correlations of the type shown in Fig. 8 were obtained in the six dogs in which technically adequate pressures were recorded.

The strength of Vs’. When the strength of Vs’ was increased or decreased beyond the value that was barely successful or unsuccessful in ventricular capture, A’ ceased to exert any influence on Vs’ regardless of the stimulation pattern used. With reductions in strength, all Vs’ failed; with increases, all succeeded.

Discussion

These experiments have shown that a suitably timed atria1 systole can frequently and consis- tently alter the efficacy of ventricular capture by a low voltage stimulus delivered to the right ventricular endocardium through a bipolar pacing catheter. The results support the idea that this phenomenon is mediated by the mechanical effects of the atria1 beat. Without changing the

25

Fig. 8. Atria1 pressure and efficacy of VB’. Abscissa: right atria1 pressure (RAP) in mm. Hg. Ordinate: the per cent of Vs’ (occurring at any given level of pressure) that was successful in ventricular capture. (A): Facilitation, total number of Vs’ = 303. (o ): Inhibition, total number of Vs’ - 666. Experi- ment performed on March 2, 1977.

appearance or timing of the atria1 depolarization, weakening of the contraction abolishes a pre- existing atria1 influence, and enhancement of the contraction establishes an influence where none existed before.

Electrotonic hypethesis. Most earlier reports favored an electrotonic mechanism as the explanation for the influauce of atria1 activity on the efficacy of pacemaker capture. This hypothesis has been reviewed and analyzed recently.1 It is very unlikely that an electrotonic mechanism was operative in the experiments described here because of the distance separating the atria and the pacing electrode. Because the space constant of the myocardium is very short,5 an electrotonic currant originating in the atria would be virtually extinguished before it reached the electrode in the right ventricle.

MscrhJlnicaI hypothasis. Several authors have acknowledged the possibility of a mechanical explanation, but few have favored it.’ This hypothesis preposes that atria1 systoie alters the efficacy of capture by increasing or decreasing the contact between the electrode tip and the ventricular myocardium. An atria1 contraction could move the intra-atria1 portion of the catheter if the catheter were in close proximity to the atria1 wall. Alternatively, by augmenting left ventricular diastolic volume, atria1 systole could move the ventricular wall relative to the catheter. This hypothesis has received some support from the report of Freston,g who radiographically observed

April, 1978, Vol. 95, No. 4

Atria1 systole and failing pacemakers

Table I. Summary of the experiments in which interpolation of A’ ’ ’ enhanced the hemodynamic performance of A’

A’ ’ ’ absent A’ ’ ’ present Absent us present

Date of Per cent Vs’ Average Per cent Vs’ Average experiment successful RAP +- SD successful RAP k SD p value

Facilitation 4/15/v 00 (O/24) 4.3 + 0.3 80 (41151) 5.5 c 0.3 < 0.001 5/3/77 11 (13/117) 4.5 +- 0.5 92 (91/99) 6.2 + 0.7 < 0.001 5/4/77 06 (2135) 4.5 _t 0.3 94 (31/33) 4.8 k 0.5 < 0.01

< 0.001

Inhibition 4/15/77 98 (64/6.5), 5.5 k 0.5 17 (18/109) 6.3 f 0.7 < 0.001

5/3/77 79 (136/173) 5.8 f 0.5 04 (6/136) 8.5 ?I 0.7 < 0.001 5/5/77 89 (150/169) 06 (9/143) < 0.001

First three horizontal rows = facilitation of Vs’. Last three horizontal rows = inhibition of Vs’. Symbols and abbreviations: A ’ ’ ’ a&sent = control, A’ present and A’ ’ ’ absent. A ’ ’ ‘present = teat condition, both A’ and A ’ ’ ’ present. The A’-Vs’ interval was constant in each experiment. Per cent Vs’ successful = the per cent of Vs’ that ww successful in ventricular capture under the conditions

specikd. Numbera in parentheses are the actual number of Vs’succeasful and the number tested. Awmge RAP = the arithmetic average of all the right atria1 prweurea (RAP) recorded under the conditions specified. SD = standard deviation. Absent us present = statistical comparison of the efBcacy of

Vs’ and the pressure data in the two conditions.p uahe = the result. of testing efficacy with the Chi-squared test, and of testing the pre~eure data with the Chi-quared teat, the Student’s t test, and the Wilcoxon z value. For each experiment every statistical test gave p < 0.001, except for the experiment of May 4, 1977, in which the Chi-square test and Student’s t test for pressure data gave p < 0.01.

that atria1 systole caused motion of the pacing catheter in eight patients.

Interpolation experiments. In order to study these two hypotheses, the present experiments were designed to dissociate partially the mechanical and electrotonic effects of the atria1 beat (A’) immediately before the test stimulus (Vs’). Inter- polation of an atria1 beat (A”) immediately before A’ resulted in a decrease in the hemodynamic performance of A’, and, conversely, interpolation of a beat (A”‘) in the penultimate cycle resulted in an increase in the pressure generated by A’. Two observations support the idea that dissocia- tion was achieved. First, the configuration of A’ on the electrocardiogram and atria1 electrogram was unchanged after interpolation despite a significant change in the pressure generated by A’. Second, interpolation of A” or A”’ undoubted- ly caused some shortening of the action potentials of A’ as a result of the abrupt increase in atria1 rate.’ However, the mechanical effects changed in opposite directions (increase or decrease in pressure) in the two types of interpolation experiments while the electrical effects changed in the same direction (shortening of the action potentials).

These experiments showed that an atria1 depolarization by itself was insufficient to alter the efficacy of capture by the ventricular test stimulus (Vs’). This was especially apparent in the mechanical enhancement experiments in which

American Heart Journal

the normal atria1 beat (A’, control condition) did not affect the efficacy of the test stimulus (Vs’).

Atrial pressure. The enhancement or depression of hemodynamic performance seen in the interpolation experiments is a manifestation of the phenomenon of restitution& and may be studied in terms of changes in pressure. However, it almost certainly was not the atria1 pressure itself that affected the efficacy of the test stimulus. Proof that the changes in efficacy were caused by motion of the pacing catheter and/or ventricular myocardium and proof that this motion was caused by atria1 systole could h&e been obtained by measuring the movements of these structures. Technical limitations prevented such measurements. Nevertheless, the pressure measurements did verify the changes in hemodynamic performance, did correlate well with the changes in efficacy of the test stimulus ,(Fig. 8 and Table I), and did show that the atria1 influence was mediated by a mechanical mechanism.

Epicardial pacing. In an earlier study using right ventricular epicardial electrodes, Arbel and colleagues9 observed that a suitably timed atria1 beat increased the efficacy of capture by a low voltage stimulus. This preliminary report was based on a single experiment conducted in a dog without atrioventricular block. It might be argued that this observation is incompatible with the mechanical hypothesis since the stimulus was

495


delivered through epicardial electrodes. However, the mechanical hypothesis does not require gross changes in the electrode contact; depending on the type of epicardial electrode used, small changes in contact could result from atria1 systole.

Summary

In the present study, using a close bipolar electrode firmly hooked into the right ventricular epicardium, we were unable to show that atria1 systole had any effect on the efficacy of the test stimulus (Vs’). These experiments were done in three dogs with and without atrioventricular heart block. In those dogs with heart block, the stimulation pattern employed was the one illustrated in Fig. 1A; in the dogs without heart block, the pattern employed was the one used by Arbel and associates.9 In contrast, in every dog adequately studied with a bipolar endocardial pacing catheter, it was possible to show either inhibition or facilitation of the test stimulus by atria1 systole.

These results are consistent with the human case reports. In 19 of the 20 cases in which sufficient information is available, the pacing catheter was of the transvenous endocardial type.’ In the single case with an epicardial electrode, the catheter tip had migrated and was not securely fixed to the heart. Thus, both the experimental and clinical observations provide additional, indirect support for the mechanical hypothesis.

The mechanism by which atria1 systole influences the efficacy of ventricular capture by a failing pacemaker was investigated in 12 dogs with atrioventricular heart block. Atria1 systole caused facilitation of ventricular capture in eight dogs, and inhibition of capture in 10 dogs. Inter- polating atria1 extrasystoles caused an enhancement or depression of the hemodynamic performance of the atria1 systole that affected the efficacy of the pacemaker stimulus. These interpolation experiments showed that atria1 systole influenced the efficacy of capture by a mechanical mechanism and not by an electrotonic mechanism. Atria1 systole probably caused motion of the endocardial pacing catheter and/or ventricular myocardium. This motion increased or decreased the contact between the pacing electrode and the endocardium with subsequent changes in the efficacy of capture. In three dogs with pacing through epicardial electrodes, atria1 systole had no effect on the efficacy of capture.

We would like to thank Dr. Eugene Lepeschkin, who initially suggested some of these ideas.

REFERENCES

1.

2.

Clinical implications. These experimental results, combined with the radiographic observations of Preston* and the analysis indicating the applicability of the mechanical mechanism to the human cases,’ strongly suggest that the Weden- sky phenomena (facilitation and inhibition) do not explain this particular type of pacemaker arrhythmia. The examples of this arrhythmia’ represent the primary, and perhaps only, situa- tions in which these electrotonic mechanisms have been thought to occur in man. Although there is no a priori reason why the Wedensky phenomena cannot apply to human cardiac electrophysiology, further investigations are needed to document their involvement. Finally, these experiments demonstrate the importance of mechanical events in the pathogenesis of a particular rhythm disturbance. Consideration of the possibility of mechanical factors in arrhythmo- genesis may well provide additional examples in the future.

3.

4.

5.

6.

7.

Abernathy, W. S., and Lepeschkin, E.: The influence of atria1 activity on ventricular capture by failing artificial pacemakers. I. Report of two new cases and review of the literature, AM. HEART J. (In press) Spear, J. F., and Moore, E. N.: Influence of brief vagal and stellate nerve stimulation on pacemaker activity and conduction within the atrioventricular conduction system of the dog, Circ. Res. 32:27, 1973. Steiner, C., and Kovalik, A. T. W.: A simple technique for production of chronic complete heart block in dogs, J. Appl. Physiol. 25:631, 1966. Alder, H. L., and Roessler, E. B.: Introduction to proba- bility and statistics, San Francisco, 1972, W. H. Freeman and Company, pp. 156, 175,231. Bigger, J. T., Jr.: Electrical properties of cardiac muscle and possible causes of cardiac arrhythmias, in Cardiac arrhythmias, Dreifus, L. S., and Likoff, W., eds., New York, 1973, Grune & Stratton, Inc., p. 13. Preston, T. A.: (Letter to editor) Late supernormal excitation, Am. J. Cardiol. 38:403, 1976. Hoffman, B. F., and Cranefield, P. F.: Electrophysiology of the heart, New York, 1960 McGraw-Hill Book Company, Inc., chapter 3, p. 50. Meijler, F. L., Nieuwendijk, E. S., and Durrer, D.: Physiological basis of paired stimulation potentiation, in Paired pulse stimulation of the heart, Cranefield, P. F., and Hoffman, B. F., eds., New York, 1966, The Rocke- feller University Press, p. 65. Arbel. E. R.. Langendorf. R.. Pick. A.. and Katz. L. N.: The effect df a&al depolarization on the resp&e to subthreshold stimulation of the ventricles. A preliminary report of clinical and experimental observations, in Paired pulse stimulation of the heart, Cranefield, P. F., and Hoffman, B. F., eds., New York, 1968, The Rocke- feller University Press, p. 32.

496 April, 1978, Vol. 95, No. 4

the influence of atrial systole on ventricular capture by failing artificial pacemakers. ii....

Documents